Paper

OSA
(Obstructive sleep apneu)

Presented By:
Dinda Murni Juniayu (20360135)
Eka Saptaning W.F (20360139)
Eliska Yanti (20360140)

Supervisor:
dr. Arman Simanjuntak, Sp.THT-KL (K) Rhinology

RSU HAJI MEDAN

MEDICAL FACULTY OF
MALAHAYATI UNIVERSITY
2021
 LIST OF CONTENT

Hal
TITLE PAGE ........................................................................................................................ i
LIST OF CONTENT............................................................................................................ ii

CHAPTER I INTRODUCTION....................................................................................1
CHAPTER II LITERATURE REVIEW
2.1. Definition..........................................................................................................2
2.2. Etiology.............................................................................................................2
2.3. Epidemiology....................................................................................................4
2.4. Sign and symptom.............................................................................................5
2.5. Pathophysiology................................................................................................6
2.6. Classification.....................................................................................................8
2.7. Diagnostic.........................................................................................................8
2.8. Treatment/Management..................................................................................12
2.9. Prognosis.........................................................................................................14
2.10. Complication.................................................................................................14

CHAPTER III CONCLUSION....................................................................................15

REFERENCES
 CHAPTER I
INTRODUCTION

Sleep apnea is the onset of abnormal episodes of respiratory rate

associated with narrowing of the upper airways in a sleep state which can be in
the form of respiratory arrest (apnea) or decreased ventilation (hypopnea). Sleep
apnea is characterized by cessation of air flow in the nose and mouth during
sleep and lasts more than 10 seconds, occurs repeatedly, can reach 20-60 times
per hour, and is accompanied by a decrease in oxygen saturation of more than
4%. There are three types of apnea / hypopnea, namely the obstructive type
(Obstructive Sleep Apnea / OSA) which is the cessation of airflow but the
respiratory effort remains, the central type (Cental Sleep Apnea / CSA) is the
cessation of airflow and respiratory effort simultaneously and the mixed type
(Mixed Sleep Apnea). apnea/MSA) which is a mixture of the two.1
OSA is one of the most common forms of sleep-related breathing
disorders. It is estimated that more than 12 million adults in America experience
OSA more often in men with a ratio of about 24% of men and 9% of women or
about 1 in 25 middle-aged men suffering from OSA, and for 1 in 50 middle-aged
women. OSA is a recurrent narrowing of the throat during sleep either partially
or completely that blocks airflow. This blockage can cause breathing problems,
or can even stop breathing for 10 to 20 seconds or more, and several times each
night, there are also symptoms of snoring (snoring), daytime drowsiness,
sleeplessness, headaches in the morning days,emotional and mental disorders.1,2
OSA is emerging as a potential causative factor for several
cardiovascular diseases. These conditions include hypertension, coronary artery
disease, myocardial infarction, heart failure and stroke, and pulmonary
hypertension. Excessive sleepiness during the day due to OSA can cause
sufferers to fall asleep suddenly so that it interferes with work and can cause
accidents.3,4

1
 CHAPTER II
LITERATURE REVIEW

2.1 Definition
OSA is a disease characterized by periodic collapse of the upper airways
during sleep which results in apnea (cessation of airflow for 10 seconds causing
a 2-4% decrease in oxygen saturation) and hypopnea (a decrease in airflow of at
least 30-50 minutes). % decrease in oxygen saturation) or both with a period
between 10 and 30 seconds, due to repeated total or partial obstruction of the
upper airway during sleep during NREM (Non Rapid Eye Movement) or REM
(Rapid Eye Movement) causing airflow to the lungs becomes obstructed and
causes a sudden reduction in blood oxygen saturation with oxygen levels falling
by as much as 40 percent or more in severe cases.1

2.2 Etiology
 Obesity

Approximately 80% of OSAS patients are obese. Obesity is one of the

predisposing factors for OSAS. There is a close relationship between body mass
index and the incidence of OSAS. A 10% increase in body weight will increase
the AHI by 32% and increase the incidence of OSAS by 6 times. Meanwhile, a
weight loss of 10% can lead to a 26% decrease in AHI. Obesity causes
narrowing of the upper respiratory tract due to excessive accumulation of fatty
tissue in the pharynx. Although there is a close relationship between obesity and
OSAS, it is important to note that not all obese subjects have OSAS. 5,6,7

 Age

Several studies have shown a high prevalence of OSAS in old age.

Research conducted by the Sleep Heart Health Study showed that 25% of men
and 11% of women had a high AHI in the 40-98 year age group. The peak age
of patients diagnosed with OSAS for the first time in general is at the age of 50
years. However, the relationship between age and OSAS is still controversial

2
 3

because of the many confounding factors and other diseases that contribute to
the occurrence of OSAS. 5,6,7

 Gender

Several epidemiological studies have reported that OSAS is more

common in men than women. In addition, there are several hypotheses that
explain the relationship between sex and the onset of OSAS, among others due
to hormonal effects that can affect the musculature of the upper respiratory tract,
differences in fat distribution and differences in pharyngeal structure and
function. 5,6,7

 Size of neck circumference

Neck circumference size is a strong predictor and is one of the

characteristics of physical examination in patients with OSAS. Neck
circumference is the measurement of the neck that crosses the upper limit of the
cricothyroid membrane as measured in the standing position. The study reported
that the mean neck circumference in OSAS patients was 43.7 cm while in non-
OSAS patients it was 39.6 cm. Another study reported that neck circumference
(>42.5 cm) was associated with an increase in AHI.8,9

 Upper airway structural abnormalities

Several studies have shown that there are anatomical structural

abnormalities in craniofacial that have an impact on the narrowing of the upper
respiratory tract. In general, there are abnormalities in the mandible, maxilla,
and hyoid bone. Small mandibles (micrognatia) and retrognathia are risk factors
for OSAS. Micrognatia and retrognatia will cause the soft palate, tongue and
soft tissue around the pharynx to be pushed posteriorly so that the airway will
narrow. In addition, the position of the maxilla that is too posterior can also be a
risk factor for OSAS. This occurs because the hard palate and soft tissues around
the pharynx are pushed posteriorly so that the size of the airway lumen
decreases. Abnormalities in the hyoid bone can lead to OSAS. Hyoid that is too
inferior will cause the tongue to be pulled posteriorly because the hyoid is one of
the insertions of the tongue-forming muscles. Abnormalities in the tonsils which
 4

are one of the lymphoid tissues in the upper respiratory tract can cause OSAS.
Tonsil hypertrophy can cause OSAS, especially in children. 10,11
Table 1. OSA risk factor12
Risk factors that play a role in OSA Translated fro
General  Obesity (BMI > 30 kg/m2) Indonesian to English
 Gender (Male > Female )
 Family history of OSA
 Post-menopause
Genetic or congenital  Down syndrome
 Pierre-Robin . syndrome
 Marfan Sindrom syndrome
Nasal/pharyngeal abnormalities  Rhinitis
 Rice polyps
 Tonsil and adenoid hypertrophy
 Nasal septal deviation
Other diseases  Acromegaly
 Hypothyroidism
Upper airway structural abnormalities  Neck circumference > 40 cm
 Temporomandibular joint
abnormalities
 Micrognathia
 Retrognathia
 Macroglossia
 palatal abnormalities
 Craniosynostosis

2.3 Epidemiology
OSA can occur in any age group, but there is an increasing prevalence
between middle age and old age with the prevalence increasing to at least 1 in 10
people among people over 65 years of age.13

Prevalence rates in adults with OSA show different results in each

country. However, it can be estimated around 3 - 7% for adult males and 2-5%
for adult females in the general population.13

In addition, the prevalence of OSA in Caucasian and Asian ethnicities

shows approximately the same number, this explains that this is a frequent
occurrence not only in developed countries but also in developing countries.13
 5

Various epidemiological studies have been carried out, especially in

developed countries, finding the incidence of OSA which is often associated
with various diseases such as diabetes mellitus, stroke, polycystic ovary
syndrome, congestive heart failure, and coronary artery disease. 14

2.4 Sign And Symtom

 Snoring

Clinically, most OSAS patients have symptoms of snoring during sleep.

Snoring is the key to the main diagnosis of OSAS obtained from the history.
This symptom of snoring is followed by episodes of not breathing (apnea) and
most often occurs in the supine sleeping position. The mechanism of snoring is
due to resistance in the upper respiratory tract accompanied by increased work
of breathing causing vibrations in the pharyngeal area. 14

 Excessive sleepiness during the day

The second most common symptom after snoring is excessive daytime

sleepiness or Excessive Daytime Sleepiness (EDS). EDS is caused by decreased
quality of sleep at night due to intermittent sleep (sleep fragmentation),
associated with repeated central nervous responses due to respiratory
disturbances during sleep. More severe symptoms can cause the patient to fall
asleep while doing activities such as watching television, eating, or while
driving. These symptoms cannot be assessed quantitatively because patients
often have difficulty distinguishing drowsiness from fatigue. Nearly 30% of men
and 40% of adult women with AHI values >5x/hour complained of not feeling
refreshed when they woke up. It is reported that 25% of men and 30% of adult
women complain of experiencing excessive sleepiness during the day.14

 Other night symptoms

Other symptoms experienced by OSAS patients at night are abnormal motor

movements, nightmares, a feeling of shortness of breath at night and nocturia. 15
 6

 Other daytime symptoms

Other symptoms experienced by OSAS patients during the day can

include headaches, feeling unrefreshed when awake, changes in behavior,
decreased concentration, depression, anxiety, impotence and decreased libido.
All of these symptoms can lead to a decrease in the patient's quality of life.15

2.5 Pathophysiology
There are three factors that play a role in the pathophysiology of OSA, namely:

The first factor is airway obstruction in the pharyngeal area due to pushing
the tongue and palate back which can cause occlusion of the nasopharynx and
oropharynx, which causes airflow to stop, even though breathing is still ongoing
during sleep. This results in apnea, asphyxia, until a short period of arousal or
awakening from sleep and an improvement in upper airway patency so that
airflow can be resumed. With improvement of asphyxia, the patient goes back to
sleep until the next event occurs again.16

Airway obstruction in OSA patients

The second factor is the size of the pharyngeal lumen formed by the
pharyngeal dilator muscles (medial pterygoid m., m. tensor veli palatini, m.
genioglosus, m. geniohyoid, and sternohyoid m.) which function to maintain the
balance of pharyngeal pressure in the event of negative intrathoracic pressure
due to diaphragm contraction. Abnormalities of neuromuscular control function
in pharyngeal dilator muscles contribute to airway collapse. Defects in
 7

ventilation control in the brain result in failure or delay of the pharyngeal dilator
muscle reflex, when the patient has periods of hypopneic apnea. 3,13,14,15

The upper airway collapses when the negative pharyngeal pressure during
inspiration exceeds the stabilizing forces of the upper airway dilator and
abductor muscles. Some patients with narrowing of the airways due to
micrognathia, retrognathia, adenotosyl hypertrophy, magroglossia or
acromegaly. Reduction in the size of the oropharynx causes upper airway
complaints to increase so that it tends to collapse if there is negative pressure.
3,13,14,15

On awakening, upper airway muscle activity is greater than normal,

possibly compensating for constriction and high airway resistance. Decreased
muscle activity during sleep causes upper airway collapse during inspiration.
Physiological reduction of upper airway activity occurs during REM sleep.
Alcohol and sedative drugs cause depression of upper airway muscle activity
leading to collapse. 3,13,14,15

Some patients also experience symptoms of nasal obstruction. High

resistance predisposes to upper airway collapse because negative pressure
increases in the pharynx during inspiration causing increased diaphragmatic
contraction to overcome the resistance to airflow in the nose. In normal people,
the size and length of the soft palate, uvula and large tongue, upper respiratory
tract at the level of the nasopharynx, oropharynx and hypopharynx are normal in
size and contour (figure 3). 3,13,14,15

Normal upper airway compared with snoring sufferers3

The third factor is craniofacial abnormalities from the nose to the

hypopharynx which can cause narrowing of the upper airway. Abnormalities of
this area can cause high resistance. This resistance also predisposes to upper
 8

airway collapse. Nasopharyngeal collapse was found in 81% of 64 OSA patients

and 75% of them had more than one upper airway narrowing.3,13,14,15

Obesity also plays a role in airway narrowing. Excess body weight on the
chest wall and diaphragmatic dysfunction impair ventilation efforts during sleep
and fatty tissue in the neck and tongue narrows the airway diameter which
predisposes to premature closure when muscle tissue relaxes during sleep. 3,13,14,15

2.6 Classification
The OSA grade classification is based on the Apnea Hypopnea Index
(AHI) value set by The American Academy of Sleep Medicine. The AHI is an
index used to assess the severity of OSA based on the number of apneas and
hypopneas that occur per hour or can be formulated as the number of apneas
plus hypopnea divided by the total sleep time. AHI is grouped into 3 groups:1
1. Mild (AHI value 5-15).
It usually manifests as drowsiness during activities that require little attention,
such as watching TV or reading.
2. Moderate (AHI value 15-30).
Usually the manifestation that appears in the form of drowsiness during
activities that require attention, such as meetings or presentations.
3. Weight (AHI value > 30).
Usually the manifestation that appears is drowsiness during activities that
require more active attention, such as talking or driving

2.7 Diagnostic
The diagnosis of OSA is established by taking a history regarding sleep
patterns, physical examination, radiological examination and special
investigations. The combination of accurate data from a good history and physical
examination can lead to indications for conducting an OSA gold standard
examination.15,17

2.7.1 History
 9

The main symptom of OSA is daytime hypersomnolence. These symptoms

cannot be assessed quantitatively because patients often have difficulty
distinguishing drowsiness from fatigue. Nearly 30% of men and 40% of adult
women with AHI values >5x/hour complained of not feeling refreshed when they
woke up. It is reported that 25% of men and 30% of adult women complain of
experiencing excessive sleepiness during the day. 15,17
Epworth sleepiness scale (ESS)and the Stanford sleepiness scale (SSS) is a
quick and easy questionnaire to assess symptoms of drowsiness. This scale is not
directly related to the AHI score index. The cause of daytime hypersomnolence is
due to intermittent sleep, associated with repeated central nervous responses due
to sleep disturbances.15.17
The EES and SSS questionnaires can be used to ask complaints related to
OSA symptoms. ESS is used to assess how sleepy the patient is and how sleepy
the patient is in daily activities, while the SSS is to determine how sleepy the
patient is in these activities. Multiple sleep latency testing (MSLT) is an objective
test to evaluate the severity of excessive daytime sleepiness. The examiner should
also ask the patient about the experience of awakening from sleep due to choking,
snoring (you can ask a bed partner) and waking up from sleep feeling
unrefreshed.15,17
 10

15
Table 2. Epworth sleepiness scale

2.7.2. Physical examination

Things that must be assessed on physical examination are BMI, neck
circumference size, nasal cavity condition (septal deviation, turbinate
hypertrophy, polyps, adenoids), Mueller's maneuver (to assess velooropharyngeal
narrowing), Friedmantounge position assessment (Mallampati modification),
palate shape mole, uvula shape, palatal flutter, palatal floppy, tonsil size and
lateral peritonsil narrowing. Adult population with BMI >30 kg/m2 had OSA
prevalence >50%. Please note that BMI and neck circumference assessments do
not have predictive abilities in women. Snoring has a positive predictive value
(PPV) of 63% and a negative predictive value (NPV) of 56% in OSA. Oximetry
examination at night as a screening for OSA has a sensitivity of 31%.17
To facilitate the assessment of the upper airway, Friedman standardized the
examination of the naso-velo-oropharyngeal area. There are four degrees of
Friedman tone position.15
The patient opened his mouth without removing his tongue. Observations
were made: grade I, the entire uvula was visualized; grade II, uvula visualized but
tonsils not visible; grade III, soft palate visualized, but uvula not visible; grade IV,
only the hard palate is visualized. This examination can predict the presence or
absence of OSA.17

2.7.3. Supporting investigation

The Mueller maneuver, performed while awake, can reflect the snoring state
of OSA patients during sleep and can be used to predict the success of
uvulopalatopharyngealplasty (UPPP) surgery. The trick is in a sitting position,
performed a nasoendoscopy and the patient is instructed to do a strong inspiration
while closing the nose and mouth. In this examination, the upper airway area was
assessed in the retropalatal and retroglossal spaces. Narrowing of this space can
occur anteroposteriorly, laterolaterally or concentrically Sleep endoscopy
examination is used to visualize airway obstruction while the patient is sleeping.
 11

There are five areas that need attention, namely: soft palate, lateral pharyngeal
wall, palatine tonsils, lingua tonsils / tongue base and epiglottis. The degree of
obstruction is divided into four categories. Simple palatal snoring, the sound of
snoring comes from vibrations of the soft palate, the walls of the velopharyngeal
sphincter and the upper oropharynx. Lateral wall collapse, the cause of obstruction
comes from the oropharynx and palatine tonsils. Tongue base / epiglottis,
velopharyngeal sphincter function is good, obstruction is at the base of the tongue
or due to hypertrophy of the lingual tonsil. The epiglottis may have contributed to
snoring. Multi segmental collapse, obstruction appears at several anatomical
levels. 18,19,20
Cephalometry and upper airway plain radiographs can be used to evaluate
craniofacial anatomic abnormalities. Computer tomography and magnetic
resonance imaging (MRI) can also facilitate understanding the relationship
between craniofacial anatomic abnormalities and respiratory disorders. 15,17
Polysomnography (PSG) is the gold standard for diagnosing OSA. PSG is a
diagnostic test to evaluate sleep disturbances that is carried out at night in a sleep
laboratory, used to assist in the selection of therapy and evaluation of the results
of therapy. There are three main signals that are monitored, namely first, signals
to confirm the state of the sleep stage such as electroencephalogram (EEG),
electrooculogram (EOG) and submental electromyogram (EMG). The second
signal is a signal related to heart rhythm, namely an electrocardiogram (ECG) and
a third signal related to respiration such as airflow (nasal thermistor technique),
oximetry, snoring, capnography, intercostal EMG, balloon esophageal
manometry, thoraco-abdominal effort, nasal pressure transducer, face mask
pneumotachography and PCO2.1,2,15 .
Levels characteristics of OSA at the time of PSG are repeated reductions in
oxygen saturation, partial or complete obstruction of the upper airway
accompanied by 50% decrease in respiratory amplitude, increased respiratory
effort resulting in changes in the stage of sleep becoming shallower and oxygen
desaturation occurring. 1,2,17
Examination with a portable monitor (PM) can be done outside the
laboratory as an alternative to PSG examination in patients suspected of having
 12

moderate to severe OSAS. Equipment varies from single channel oximeter to

complete PSG. In general, PM measures several parameters such as oxygen
saturation, respiratory and cardiac systems, activity sleep/awake, but most do not
record EEG. The PM has biosensors to at least measure airflow, effort to breathe,
and blood oxygenation. The diagnosis and grade of OSAS were determined
according to the same criteria as PSG. If the PM examination in a patient
suspected of having OSAS fails or is inadequate, a PSG examination must be
carried out in the laboratory. 1,2,17
2.8 Treatment / Management
OSA management consists of nonsurgical therapy and surgical therapy.
1. Non-surgical therapy can be done with lifestyle modification, use of oral
appliance (OA) and CPAP.
 Lifestyle modification by losing weight because OSA patients with
obesity can increase the volume and function of the upper respiratory
tract. Avoiding alcohol, sedatives, nicotine and caffeine at night can
improve upper airway muscle tone and central respiratory mechanisms.
Ephedrine preparations, although not providing long-term effects,
Patients with mild to moderate OSA who cannot use CPAP or who do
not have success with CPAP can take OA. This device repositions the
anatomy of the upper airway to prevent obstruction by widening the
airways, stabilizing the maxilla forward, and widening the soft palate and
tongue.
 OA consists of the Mandibular Advancement Device (MAD) which
pushes the lower jaw forward to keep the airway open and the Tongue
Retaining Device (TRD) which holds the tongue in position to keep the
airway open. Some complications that may occur are pain at night, dry
lips, discomfort in the teeth. With long-term use, permanent changes in
the position of the teeth or jaws may occur. Contra indications for the use
of OA are arthritis of the jaw joint, poor dental conditions, nasal
obstruction, poor patient motivation, pharyngeal stenosis. The use of OA
provides significant improvement in AHI, minimal oxygen desaturation,
 13

minimal arousal index, few side effects, good patient acceptance and
comfort after 6 months of use.1,2,15,17
 The use of CPAP is the non-surgical treatment of OSA that is considered
the most effective for reducing symptoms of snoring, apnea-hypopnea
and daytime hypersomnolence. Weaknesses of CPAP are discomfort
during use, claustrophobia, headaches, rhinitis, facial and nasal irritation
and aerophagia.17,19
2. The goal of surgical therapy in OSA is to improve the volume and shape of the
upper airway. Indications must be clear and well prepared. Indications for OSA
surgery are AHI 20, O2 saturation <90%, esophageal pressure below -10
cmH2O, the presence of cardiovascular disorders (such as arrhythmias and
hypertension), neuropsychiatric symptoms, failure with nonsurgical therapy and
the presence of anatomic abnormalities that cause airway obstruction. No one
technique is really good for OSA.1,2
 Uvulopalatopharyngoplasty (UPPP) is one of the surgical techniques by
performing excision on the inferior margin of the soft palate including
the uvula and tonsils. According to meta-analysis studies that have been
carried out, it is stated that UPPP can significantly reduce AHI and
increase oxygen saturation. UPPP is less effective in elderly patients and
high BMI.1,2,19
 Genioglossus advancement can correct retroglossal obstruction. This
technique is performed in patients with AHI >30 caused by obstruction at
the base of the tongue. The success of this technique in improving AHI
and oxygen saturation is 66-85%. 1,2,18
 The maxilla-mandibular osteotomy technique can be performed in
patients who have not progressed post-UPPP and genioglossus
advancement after being evaluated for six months with PSG. This
technique has a 97-100% success rate in reducing AHI and increasing
blood oxygen saturation. 1,2,18
  Laser-assisted uvuloplasty (LAUP) is a technique similar to UPPP, but
uses a laser (CO2, argon). This technique can be performed under local
anesthesia in 1-3 outpatient sessions. LAUP is not recommended in
 14

patients who have tonsillar obstruction, thickened pharyngeal mucosa,

tonsillar hypertrophy and AHI >30. LAUP is now rarely done. 1,2,19
 Another surgical technique is radiofrequency ablation (RA) of the palate.
Indicated for patients with obstruction of the palate and AHI <15. The
success rate of RA palate in eliminating complaints of snoring and
improving the ESS value is 75%, but does not change the AHI value. 1,2,16
2.9 Prognosis
Based on the recommendations of the Scottish Intercollegiate Guidelines
Network (SIGN) based on research, patients who have a fairly good therapeutic
success rate are patients with AHI 15 and patients with a decrease in oxygen
saturation of 4% by >10 times per hour. Improvements can be seen from
reduced daytime drowsiness, improved driving with simulation, quality of life,
blood pressure, and emotional stability.20 Untreated OSA can result in
neurocognitive impairment, whereas in patients who respond well to CPAP, the
short-term prognosis is good. 4-8 weeks of treatment provides better general
health status, improved cognitive function, reduced snoring and daytime
sleepiness. Therapy can significantly reduce the risk of cardiovascular
complications, especially in patients with severe OSAS. Reduction in clinical
symptoms with surgical procedures does not always correspond to a reduction in
apnea, nor does a decrease in daytime sleepiness necessarily mean the loss of
OSA. therefore patients should be monitored periodically with PSG to ensure
the effectiveness of therapy.19
2.10 Complications
The consequences if OSA is not treated can be divided into 2 categories,
namely:
1. Sleep disturbances: poor performance at work, decreased short-term memory,
work and motor vehicle accidents (OSA patients have a risk of 15 times more
frequent motor vehicle accidents than the general population), loss of energy
throughout the day, headaches in morning sickness, weight gain, mood disorders
and depression, impotence and decreased sexual intercourse.22,23,24
2. Hypertension (in 50% of OSA patients) which if OSA remains untreated then
the incidence of hypertension will increase the risk for a heart attack or stroke),
 15

cardiac arrhythmias, and stress on the cardiovascular system because OSA

causes the heart and lungs to work harder. Hypertension that occurs in patients
who are undiagnosed or not receiving OSA treatment can be difficult to treat,
and various consequences will occur. This requires that effective OSA treatment
will improve and control blood pressure in some patients.1,17,20
 CHAPTER III
CONCLUSION

Obstructive sleep apnea (OSA) is a disease characterized by periodic

collapse of the upper airway during sleep resulting in apnea and hypopnea or
both with a period of between 10 and 30 seconds due to repeated total or partial
obstruction of the upper airway. during sleep during NREM or REM sleep.
OSA can occur in any age group, but the prevalence increases between
middle age and old age with prevalence increasing to at least 1 in 10 among
people over 65 years of age. The etiology of OSA is a complex condition that
affects each other in the form of neural, hormonal, muscular and anatomical
structures that cause upper respiratory tract collapse. OSA grade classification
based on the value of the Apnea Hypopnea Index (AHI). Factors that play a role
in the pathogenesis of OSA are airway obstruction in the pharyngeal area due to
pushing the tongue and palate backwards which can cause occlusion of the
nasopharynx and oropharynx, pharyngeal lumen size, and craniofacial
abnormalities from the nose to the hypopharynx.
The diagnosis of OSA is established by taking a history regarding sleep
patterns, physical examination, radiological examination and special
investigations. The combination of accurate data from a good history and
physical examination can lead to indications for carrying out the gold standard
OSA examination in the form of a night sleep examination with a
polysomnography / PSG tool. Therapy to treat sleep disturbances in OSA can be
divided into style changes, use of devices, and surgical intervention.
CPAP physiologically works as a pneumatic splint that maintains upper
airway patency during inspiration and expiration. The result is a decrease in
impaired gas exchange, blood pressure and arousal, which plays a role in
reducing the incidence of airway obstruction. Due to its ease of use and proven
effectiveness, CPAP is considered the first-line therapy for severe OSA.

16
 17

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